NF-?B in critical diseases: a bad guy?

Senftleben, Uwe

doi:10.1007/s00134-003-1932-7

Cited by 10 publications

(5 citation statements)

References 28 publications

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“…Indeed, PDTC was shown to have the potential of targeting such molecules as mitogen‐activated protein kinases (MAPK) p38 and c‐Jun N‐terminal (JNK) kinase, the activator protein‐1 (AP‐1) transcription factor and the heat shock transcription factor 1 (HSF1) (see references in Senftleben, 2003), p53 (Iseki et al, 2000a; Wu and Momand, 1998), and a number of molecules acting in oxidative stress‐activated signaling pathways such as zinc (Kim et al, 2003a, 2003b), copper (Iseki et al, 2000a, 2000b), and glutathione (Kim et al, 2003b). A mechanistic role of p53 in CP teratogenesis has been demonstrated (Moallem and Hales, 1998; Mikheeva et al, 2004) and such a role is also conceivable for all the above‐mentioned molecules, except maybe p38 and JNK, which were suggested to not be involved in the teratogenic response to CP (Mirkes et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Differential teratogenic response of TNFα^+/+ and TNFα^−/− mice to cyclophosphamide: The possible role of NF‐κB

Torchinsky

Gongadze²,

Savion

et al. 2006

Birth Defects Research

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BACKGROUND:We observed previously that tumor necrosis factor a (TNFa)-knockout embryos are more sensitive to a cyclophosphamide (CP)-induced teratogenic insult than their TNFa-positive counterparts, implicating molecules acting in TNFa-activated antiapoptotic pathways in the mechanisms underlying this phenomenon. The main goal of this study was to assess whether the transcription factor nuclear factor jB (NF-jB) may be 1 of those molecules. Such a choice is based by evidence demonstrating TNFa as a powerful activator of NF-jB and a key role of the transcription factor in the most effective TNFa-activated antiapoptotic cascade. Also, the expression pattern of active caspases 3, 8, and 9 was researched to assess the sensitivity of TNFa þ/þ and TNFa À/À embryos to CP-induced apoptotic stimuli. METHODS: TNFa-knockout mice were exposed to CP on day 12 of pregnancy, with or without an NF-jB inhibitor, pyrrolidine dithiocarbamate (PDTC) and sacrificed on day 18 of pregnancy to evaluate the CP-induced teratogenic effect. Embryos harvested 24 or 48 hr after the CP treatment were used to evaluate NF-jB DNA-binding and activity of caspases 3, 8, and 9. RESULTS: PDTC potentiated the CP-induced teratogenic effect and augmented the CPinduced suppression of NF-jB DNA-binding. These effects were more prominent in TNFa À/À than TNFa þ/þ embryos. CP-induced caspase activation was found to be similar in TNFa À/À and TNFa þ/þ embryos at 24 hr after treatment. At 48 hr, TNFa À/À embryos exhibited higher levels of active caspases 8 and 9 than their TNFa-positive counterparts. CONCLUSIONS: The results of our study allow us to hypothesize that NFjB may be a component of mechanisms underlying differential sensitivity of TNFa À/À and TNFa þ/þ mice to CP-induced teratogenic insult.

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Section: Discussionmentioning

confidence: 99%

Differential teratogenic response of TNFα^+/+ and TNFα^−/− mice to cyclophosphamide: The possible role of NF‐κB

Torchinsky

Gongadze²,

Savion

et al. 2006

Birth Defects Research

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“…For example, previous studies have shown that NF-κB translocation participates in the up-regulation of LPS-induced iNOS, IL-6 and TNF-α expression [ 2 , 18 ]. Thus, the blocking of the initial nuclear translocation of NF-κB could prevent the development of sepsis [ 33 ]. Recent studies in murines have shown that propofol inhibits the nuclear translocation of NF-κB in LPS-induced macrophages, leading to transcriptional suppression of a large number of downstream genes [ 13 ].…”

Section: Discussionmentioning

confidence: 99%

Propofol attenuates LPS-induced tumor necrosis factor-α, interleukin-6 and nitric oxide expression in canine peripheral blood mononuclear cells possibly through down-regulation of nuclear factor (NF)-κB activation

Pei

Wang

2015

The Journal of Veterinary Medical Science

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Sepsis is a major cause of mortality in intensive care medicine. Propofol, an intravenous general anesthetic, has been suggested to have anti-inflammatory properties and able to prevent sepsis induced by Gram-positive and Gram-negative bacteria by down-regulating the gene expression of pro-inflammatory cytokines. However, propofol’s anti-inflammatory effects upon canine peripheral blood mononuclear cells (PBMCs) have not yet been clarified. Here, we isolate canine PBMCs and investigate the effects of propofol on the gene expressions of both lipopolysaccharide (LPS)-induced interleukin-6 (IL-6) and tumor necrosis factor (TNF)-α and upon the production of nitric oxide (NO). Through real-time quantitative PCR and the Griess reagent system, we found that non-cytotoxic levels of propofol significantly inhibited the release of NO and IL-6 and TNF-α gene expression in LPS-induced canine PBMCs. Western blotting revealed that LPS does significantly increase the expression of inducible NO synthase (iNOS) protein in canine PBMCs, while pretreatment with propofol significantly decreases the LPS-induced iNOS protein expression. Propofol, at concentration of 25 µM and 50 µM, also significantly inhibited the LPS-induced nuclear translocation of nuclear factor (NF)-κB p65 protein in canine PBMCs. This diminished TNF-α, IL-6 and iNOS expression, and NO production was in parallel to the respective decreased NF-κB p65 protein nuclear translocation in the LPS-activated canine PBMCs pretreated with 25 µM and 50 µM propofol. This suggests that non-cytotoxic levels of propofol pretreatment can down-regulate LPS-induced inflammatory responses in canine PBMCs, possibly by inhibiting the nuclear translocation of the NF-κB p65 protein.

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“…Zimosanın peritonal makrofajlarda TNF-α transkripsiyonunun düzenlenmesinde kritik rol oynayan transkripsiyon faktörü, nükleer faktör κB (NF-κB)'nin inhibitör proteini, κB inhibitörü (IκB-α)'nın degredasyonuna bağlı olarak NF-κB'yi etkinleştirdiği gözlenmiştir (22). Zimosanla oluşturulan şok-ta, NF-κB, TNF-α'ya ek olarak öteki pek çok sitokinlerin gen transkripsiyonunu da düzenlemektedir.…”

Section: Zimosanın Patofizyolojik Olaylardaki Rolüunclassified

Signal Transduction of Zymosan and Spleen Tyrosine Kinase

Ünsal¹,

Temiz²,

Tunçtan³

et al. 2014

MUSBED

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Zimosan sinyal iletisi ve dalak tirozin kinazıZimosan, Saccharomyces cerevisiae'nin hücre duvarından elde edilen, polisakkarit zincirlerinden oluşan bir bileşendir. Zimosan, başlıca 1,3-β-glukan, 1,6-β-glukan ve α-mannan gibi çapraz bağlı polisakkaritlerden oluşmaktadır. Zimosan, fungal sepsis, septik olmayan şok, çoklu organ yetmezliği, akut peritonit, irritabl bağırsak sendromu gibi enflamatuvar hastalıkların patojenezinde rol oynamakta ve ilgili deneysel modellerde kullanılmaktadır. Zimosanın monosit, makrofaj ve dendritik hücreler gibi immün sistem hücrelerindeki etkilerine toll-like receptor 2, dektin-1, mannoz ve kompleman reseptörleri gibi çeşitli reseptörler aracılık etmektedir. Dalak tirozin kinazı (Dtk), 72 kDa ağırlığında reseptör ile kenetli olmayan bir intraselüler tirozin kinazdır. Dtk'nin, mast hücreleri, nötrofiller, makrofajlar ve trombositler gibi tüm hematopoetik hücrelerde ve fibroblastlar, epitel, sinir ve damar endotel hücreleri gibi hematopoetik olmayan hücrelerde eksprese edildiği gösterilmiştir. Dtk, zimosanın dektin-1 reseptörü aracılığıyla oluşturduğu hücresel yanıtlara aracılık eden önemli bir kinazdır. Bu derlemede, zimosan sinyal iletisinde Dtk'nin rolü değerlendirilmiştir. Anahtar sözcükler: Zimosan, Dalak tirozin kinazı, dektin-1, enflamasyon ABS TRACT Signal transduction of zymosan and spleen tyrosine kinaseZymosan is a component produced by polysaccharide which is obtained from cell wall of Saccharomyces cerevisiae. Zymosan consists of crosslinked polysaccharides such as 1,3-β glucan, 1,6-β glucan, and α-mannan. Zymosan plays a role in inflammmatory diseases such as fungal sepsis, non-septic shock, multiple organ dysfunction syndrome, acute peritonitis, irritable bowel syndrome and it is used in related experimental models. Toll-like receptor 2, dectin-1, mannose, and compleman receptors mediate zymosan's effects on immune system cells such as monocytes, macrophages, and dendritic cells. Spleen tyrosine kinase (Syk) is a cytosolic, intracellular, 72-kDa protein tyrosine kinase. It is demonstrated that Syk is expressed in hematopoietic cells such as mast cells, neutrophils, macrophages, B cells, leukocytes, and platelets and in non-hematopoietic cells such as epithelial, fibroblast, neuronal cells, and vascular endothelial cells. Spleen tyrosine kinase is a critical kinase that mediates cellular responses through dectin-1 receptor by zymosan. In this review, the role of syk in is evaluated in the signal transduction of zymosan.

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NF-?B in critical diseases: a bad guy?

Cited by 10 publications

References 28 publications

Differential teratogenic response of TNFα^+/+ and TNFα^−/− mice to cyclophosphamide: The possible role of NF‐κB

Differential teratogenic response of TNFα^+/+ and TNFα^−/− mice to cyclophosphamide: The possible role of NF‐κB

Propofol attenuates LPS-induced tumor necrosis factor-α, interleukin-6 and nitric oxide expression in canine peripheral blood mononuclear cells possibly through down-regulation of nuclear factor (NF)-κB activation

Signal Transduction of Zymosan and Spleen Tyrosine Kinase

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NF-?B in critical diseases: a bad guy?

Cited by 10 publications

References 28 publications

Differential teratogenic response of TNFα+/+ and TNFα−/− mice to cyclophosphamide: The possible role of NF‐κB

Differential teratogenic response of TNFα+/+ and TNFα−/− mice to cyclophosphamide: The possible role of NF‐κB

Propofol attenuates LPS-induced tumor necrosis factor-α, interleukin-6 and nitric oxide expression in canine peripheral blood mononuclear cells possibly through down-regulation of nuclear factor (NF)-κB activation

Signal Transduction of Zymosan and Spleen Tyrosine Kinase

Contact Info

Product

Resources

About

Differential teratogenic response of TNFα^+/+ and TNFα^−/− mice to cyclophosphamide: The possible role of NF‐κB

Differential teratogenic response of TNFα^+/+ and TNFα^−/− mice to cyclophosphamide: The possible role of NF‐κB